Robust, stretchable bioelectronic interfaces for cardiac pacing enabled by interfacial transfer of laser-induced graphene via water-response, nonswellable PVA gels.

Implantable cardiac pacemakers are crucial therapeutic tools for managing various cardiac conditions. For effective pacing, electrodes should exhibit flexibility, deformability, biocompatibility, and high conductivity/capacitance. Laser-induced graphene (LIG) shows promise due to its exceptional electrical and electrochemical properties. However, the fragility of LIG and the non-stretchability of polyimide substrates pose challenges when interfacing with the beating heart. Here, we present a simple method for fabricating robust, flexible, and stretchable bioelectronic interfaces by transferring LIG via water-responsive, nonswellable polyvinyl alcohol (PVA) gels. PVA solution penetrates the porous structure of LIG and solidifies into PVA xerogel as the solvent evaporates. The robust PVA xerogel enables the smooth transfer of LIG and prevents stretching of the LIG network during this process, which helps maintain its conductivity. When hydrated, the xerogel becomes a stable, nonswellable hydrogel. This gives the LIG-PVA hydrogel (LIG-PVA-H) composites with excellent conductivity (119.7 ± 4.3Ω sq-1), high stretchability (up to 420%), reliability (cyclic stretch under 15% strain, with ∼ 1-time resistance increase), and good stability in phosphate buffered saline. The LIG-PVA-H composites were used as biointerfaces for electrocardiogram signal recording and electrical pacing on rat hearts ex vivo and in vivo, using commercial setups and a custom-built implantable wireless device. This work expands the application of LIG in bioelectronic interfaces and facilitates the development of electrotherapy for cardiac diseases.

How does leaf succulence relate to plant drought resistance in woody shrubs?

Succulence describes the amount of water stored in cells or organs, regardless of plant life-form, including woody and herbaceous plants. In dry environments, plants with greater survival often have greater leaf succulence. However, it is unclear how leaf succulence relates to plant drought resistance strategies, including isohydry (closing stomata to maintain leaf water status) and anisohydry (adjusting cell turgor to tolerate low leaf water status), which exist on a continuum that can be quantified by hydroscape area (larger hydroscape area indicates more anisohydric). We evaluated 12 woody species with differing leaf succulence in a glasshouse dry-down experiment to determine relationships among leaf succulence (degree of leaf succulence, leaf succulent quotient and leaf thickness) and plant drought response (hydroscape area, plant water use, turgor loss point and predawn leaf water potential when transpiration ceased). Hydroscape areas ranged from 0.72 (Carpobrotus modestus S.T.Blake; crassulacean acid metabolism (CAM) plants) to 7.01 MPa2 (Rhagodia spinescens R.Br.; C3 plants), suggesting that C. modestus was more isohydric and R. spinescens was more anisohydric. More isohydric species C. modestus, Carpobrotus rossii (Haw.) Schwantes and Disphyma crassifolium (L.) L.Bolus (CAM plants) had greater leaf succulence, lower root allocation, used stored water and ceased transpiration at higher predawn leaf water potential, shortly after reaching their turgor loss point. The remaining nine species that are not CAM plants had larger hydroscape areas and ceased transpiration at lower predawn leaf water potential. Greater leaf succulence was not related to cumulative water loss until transpiration ceased in drying soils. All 12 species had high turgor loss points (-1.32 to -0.59 MPa), but turgor loss point was not related to hydroscape area or leaf succulence. Our data suggest that overall greater leaf succulence was related to isohydry, but this may have been influenced by the fact that these species were also CAM plants.

Shared Molecular Mechanisms between Alzheimer's Disease and Periodontitis Revealed by Transcriptomic Analysis.

OBJECTIVE: To investigate the genetic crosstalk mechanisms that link periodontitis and Alzheimer's disease (AD). BACKGROUND: Periodontitis, a common oral infectious disease, is associated with Alzheimer's disease (AD) and considered a putative contributory factor to its progression. However, a comprehensive investigation of potential shared genetic mechanisms between these diseases has not yet been reported. METHODS: Gene expression datasets related to periodontitis were downloaded from the Gene Expression Omnibus (GEO) database, and differential expression analysis was performed to identify differentially expressed genes (DEGs). Genes associated with AD were downloaded from the DisGeNET database. Overlapping genes among the DEGs in periodontitis and the AD-related genes were defined as crosstalk genes between periodontitis and AD. The Boruta algorithm was applied to perform feature selection from these crosstalk genes, and representative crosstalk genes were thus obtained. In addition, a support vector machine (SVM) model was constructed by using the scikit-learn algorithm in Python. Next, the crosstalk gene-TF network and crosstalk gene-DEP (differentially expressed pathway) network were each constructed. As a final step, shared genes among the crosstalk genes and periodontitis-related genes in DisGeNET were identified and denoted as the core crosstalk genes. RESULTS: Four datasets (GSE23586, GSE16134, GSE10334, and GSE79705) pertaining to periodontitis were included in the analysis. A total of 48 representative crosstalk genes were identified by using the Boruta algorithm. Three TFs (FOS, MEF2C, and USF2) and several pathways (i.e., JAK-STAT, MAPK, NF-kappa B, and natural killer cell-mediated cytotoxicity) were identified as regulators of these crosstalk genes. Among these 48 crosstalk genes and the chronic periodontitis-related genes in DisGeNET, C4A, C4B, CXCL12, FCGR3A, IL1B, and MMP3 were shared and identified as the most pivotal candidate links between periodontitis and AD. CONCLUSIONS: Exploration of available transcriptomic datasets revealed C4A, C4B, CXCL12, FCGR3A, IL1B, and MMP3 as the top candidate molecular linkage genes between periodontitis and AD.